CNS Anatomy Flashcards
Inferior olivary nucleus
The inferior olivary nucleus (ION) is located in the medulla. It receives motor input from multiple sources including the red nucleus and the dentate nucleus, amongst others. The efferent projections (“climbing fibers”) extend to the Purkinje cells of the cerebellum. Given its close association with the cerebellum, lesions involving the inferior olivary nucleus result in motor incoordination. Hypertrophy of the of the ION occurs when the afferent projections from the red nucleus or dentate nucleus are interrupted. This results in trans-synaptic degeneration of the olivary neurons which appear as enlarged, vacuolated neurons surrounded by gliotic neuropil. The number of neurons is not increased. In fact, there is a loss of neurons. The increase in size is resulted from gliotic scarring and therefore the term hypertrophy may not be totally correct. It is more like a kind of pseudohyptertrophy.
The triangle of Guillain and Mollaret (also known as myoclonic triangle, dentatorubro-olivary pathway) represents the fibers extending from the red nucleus to the inferior olivary nucleus as well as the fibers between the red nucleus and the contralateral dentate nucleus. Damage to the red nucleus/ION fibers can result in hypertrophy of the ION
Nucleus acumbens
nucleus accumbens, a component of the mesolimbic pathway involved in reward reinforcement, is situated within the basal ganglia, between the caudate and putamen.
Subiculum
Transitional zone between the 6 layer neocortex and the 3 layers paleocortex. It is the primary output of the hippocampus and lies between the entorhinal cortex and the CA1 region of the hippocampus. The dentate gyrus (fascia dentata) is highlighted by the arrow. The fimbria is the major efferent track of the hippocampus.
It is particularly susceptible to hypoxic/ischemic injury, along with the CA1 and CA4 regions of the hippocampus. Volume loss occurs in the subiculum in even early stages of Alzheimer disease (AD), with a correlation between increased volume loss and longer disease survival. The hippocampus is well formed by the 16th week of gestation.
Central pontine myelinolysis
Neuroanatomical consideration: The pons is a portion of the brainstem, situated between the midbrain and the medulla. The “belly” of the pons is largely composed of corticospinal tracts seen in cross section, pontocerebellar fibers seen in longitudinal section, and pontine nuclei.
Pathology of the case: There is substantial loss of myelin (white arrow). This pattern is often described as butterfly shaped at the center of basis pontis. The distinctive feature here is that a thin rim of residual myelin is always present at the rim of the lesion. These features are most compatible with central pontine myelinolysis.
Locked-in Syndrome (LIS) is a condition in which a patient lacks voluntary control of the body but is otherwise cognitively aware. The patient cannot communicate verbally but may be able to utilize eye movements and blinking as methods of communication. Injury to the brainstem with sparing of the cerebral hemispheres explains the retained cognitive ability in the absence of voluntary motor control. It is often resulted from extensive damage of the basis pontis. This condition is not limited to CPM although it is so associated in text books. LIS can be seen in situations such as pontine stroke and trauma.
Central pontine myelinolysis (CPM) is one of many possible causes of LIS. CPM is the result of damage to the myelin sheath of axons within the pons. The most well-known cause of CPM is over rapid correction of hyponatremia in a patient with long-standing hyponatremia (presumably, the patient has adapted to this state). In these cases, correction of the serum sodium level should be done slowly to allow the body to adjust to the increased sodium levels. CPM may also be seen in patients with chronic liver disease as metabolic disturbances are a common finding in these patients.
Parinaud Syndrome
result of injury to the dorsal midbrain, either by compression (e.g. brain tumor) or ischemic injury (e.g. infarct). It results in an upward gaze palsy, pupillary light-near dissociation, and convergence-retraction nystagmus.
Anton Syndrome
(aka visual anosognosia OR cortical blindness) is the result of injury to the bilateral primary visual cortices in the occipital lobes. This injury is most often ischemic in origin (e.g. stroke) but may also be traumatic in origin. This results in blindness, though the patient often denies the inability to see, frequently confabulating to cover over the lack of sight.
Wallenberg Syndrome
(lateral medullary syndrome) is the result of injury to the lateral aspect of the medulla and results in sensory deficits of the contralateral body and ipsilateral face. Occlusion of the vertebral artery is the most common cause, though occlusion of the posterior inferior cerebellar artery (PICA) or one of its branches may also have the same effect.
Atrophy of pyramid secondary to ipsilateral resolving/resolved massive infarction of medial cerebral artery territory
One side of the pyramid is atrophic and much smaller than the other side accompanied by the loss of myelin, without other pathologic changes. These features are consistent with massive atrophic changes of the cortical spinal tract and is most commonly seen in massive destruction of the ipsilateral capsule, often due to hypertensive hemorrhage in the basal ganglia, and infarction of the ipsilateral motor area in infarction of the medial cerebral artery territory. Similar atrophic changes will be seen in the lateral and anterior cortical spinal cord as they are the extension of the crossed and non-crossed component of the pyramid. The principal motor manifestation of this type of lesion is hemiplegia. Since it takes time for this type of degeneration to occur, it is not seen at the acute phase or initial phase of the infarction but the resolving or resolved phase of the infarction.
Loss of Purkinje cells with Bergmann gliosis
Segmental loss of Purkinje cells in adults is not an uncommon findings on autopsy brains. The mechanisms are diversified that range from alcohol to minor ischemic insults that are not serious enough to endanger large neurons but not infarction. Bergman gliosis is a reactive process similar to gliosis in other part of the brain. When the condition is severe, Bergman glia can form a distinct layer. Note that the nuclei of Bergman glia have open chromatin and is larger than that of the internal granular neurons
Cajal-Retzius neurons
aka horizontal cells of Cajal. Cajal-Retzius neurons can be seen in the developing cerebral cortex and immature hippocampus. In the human cortex, they are the first large neuron to appear in the cortex. seen in the mantle or marginal zone within the cortical plate. This is a heterogeneous population reeling-producing cells. Reelin is an extracellular matrix protein that is critical in acting as the stopping signal for radial neuronal migration.
Betz cells
aka pyramidal cells of Betz are giant pyramidal neurons, about 100 μm in dimension, in the 5th cortical neuronal layer in the primary motor cortex. These are upper motor neurons.
